| Project/Area Number |
26462827
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Aichi Gakuin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
平居 貴生 愛知学院大学, 薬学部, 准教授 (80389072)
友寄 大介 (兒玉大介 / 友寄 大介(兒玉大介)) 愛知学院大学, 薬学部, 講師 (40549979)
浜村 和紀 愛知学院大学, 歯学部, 准教授 (00422767)
近藤 久貴 愛知学院大学, 歯学部, 講師 (40469002)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 交感神経 / 骨代謝 / α1B-アドレナリン受容体 / 骨形成 / 骨芽細胞 / α-アドレナリン受容体 / 神経 / α1-アドレナリン受容体 / 時計遺伝子 |
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| Outline of Final Research Achievements |
To obtain a better understanding of bone remodeling by the sympathetic nervous system, we investigated the role of alpha 1B-adrenoceptor signalling. The systemic administerion of prazosin, alpha1-adrenoceptor antagonist, decreased the bone formation in mice. In addition, alpha1B-adrenoceptor-deficient mice showed a lower bone mass due to decreased bone formation, without exhibiting any changes in bone-resorbing activity. Furthermore, the treatment of phenylephrine, alpha1-adrenoceptor agonist, with osteoblastic MC3T3-E1 cells increased the expression of the transcriptional factor CCAAT/enhncer-binding protein delta (Cebpd). The over-expression of Cebpd induced cellular proliferation in MC3T3-E1 cells, whereas the silencing of Cebpd suppressed it. These results suggested that alpha1B-adrenoceptor signalling is required for bone formation and regulated cellular proliferation through a mechanism relevant to the up-regulation of Cebpd in osteoblasts.
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